Researchers in Brazil have identified immune proteins that flood the heart tissues of many people with Chagas disease, suggesting a cause of this deadly complication of the parasitic tropical disease. The malady afflicts 18 million people in South and Central America, placing millions at risk of heart failure.

The researchers examined heart tissues from autopsies of 29 people who had Chagas disease and signs of heart damage. The team also studied heart tissue from autopsies of 12 people without Chagas but who had enlarged hearts, biopsies of 6 people living with enlarged hearts, tissue from 21 people who died without heart problems, and biopsies from 21 people with normal-size hearts.

The researchers report in the June Journal of Pathology that 11 of the 29 Chagas patients had evidence of so-called membrane-attack-complex proteins in their heart cells, whereas only 1 of the 22 people who hadn't been infected with Chagas' disease had the immune proteins in heart cells.

The Chagas patients were also more likely than the others to have high concentrations of these immune proteins in their blood vessel cells.

This is the first time anyone has documented membrane-attack-complex proteins in Chagas' disease-related heart damage, says study coauthor Vera Demarchi Aiello, a cardiovascular pathologist at the University of Sao Paulo Medical School.

The cause of the influx of these immune proteins into the heart and vessel cells is still unclear. The result of the onslaught, however, may be to attract inflammatory molecules to the heart, says Aiello.

Normally, membrane-attack-complex proteins--which belong to a group of immune agents called complement proteins--create openings in the membranes of cells targeted for destruction. In these patients, many of the proteins only partially penetrated cells. This probably stimulated heart-cell proliferation and inflammation, both of which are characteristic of heart disease in Chagas patients, Aiello says.

"In the future, such knowledge may play a role in treatment," she says.--N.S.

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